Marco Aurélio Gomes Veado
3 min read
•
September 29, 2025
The origins of dementia remain one of the greatest mysteries in neuroscience. For decades, researchers have focused on beta-amyloid plaques as the main culprit in Alzheimer’s disease. Yet, emerging perspectives suggest that the real problem may lie in the immune system itself, a case of “friendly fire,” where the brain’s own defense mechanisms mistakenly damage healthy neurons.
This MCI and Beyond’s blog article explores a provocative hypothesis: dementia may not be fully preventable and could, in fact, be the result of an autoimmune-like process triggered by genetics, lifestyle, or injury.
A common belief is that a healthy lifestyle, including a balanced diet, regular exercise, and mental stimulation, can help prevent dementia. While these factors reduce risk and may delay onset, they do not guarantee protection.
This has led some scientists to reconsider whether dementia is something that can be prevented or whether it is an inevitable outcome once specific biological “switches” are triggered.
The brain has its own immune guardians called microglia. According to Science Direct, their job is to protect neurons by removing waste, toxins, and threats such as beta-amyloid proteins. However, recent studies suggest that microglia may become overactive, leading to chronic inflammation.
Instead of protecting neurons, they start releasing toxic molecules that damage them, a classic case of immune system dysregulation.
This resembles what happens in autoimmune disorders, where the body attacks its own tissues.
Imagine a battlefield where soldiers cannot distinguish between friend and foe. In dementia, immune cells may treat healthy neurons as invaders. Instead of removing only toxic proteins, they also attack the very structures they are meant to defend.
This “friendly fire” hypothesis reframes dementia as a condition where:
If dementia is partly an autoimmune-like condition, treatment strategies might shift toward:
These approaches may not “prevent” dementia outright, but they could delay onset or reduce severity by calming the brain’s immune system.
The traditional view of dementia as simply a buildup of beta-amyloid is being challenged. Instead, the disease may involve a deeper malfunction: an immune system turned against its own neurons.
While more research is needed, this perspective highlights the importance of looking beyond plaques and considering dementia as a potential autoimmune “friendly fire” disorder.
For caregivers and families, this reinforces the value of lifestyle interventions, not as absolute prevention, but as tools to build resilience against an unpredictable biological process.
Thus, let us keep our open minds to face new approaches like that. Dementia is still a mystery, but Science may break this code as soon as we can imagine!
Disclaimer: This article presents a hypothesis inspired by current research trends. It is not medical advice. Always consult a healthcare professional for guidance on dementia risk and prevention.
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